Abstract Aims/Introduction The molecular mechanisms of diabetic nephropathy (DN) are poorly identified. However, the advantage of an increasing amount on microarray data of diabetic nephropathy intrigued us to explore the mechanisms based on bioinformatics prediction for diabetic nephropathy. Materials and Methods Bioinformatics analysis was conducted to screen the hub genes associated with diabetic nephropathy. The average human renal tubular epithelial cells were exposed to high glucose (HG) to generate an in vitro cell model. In addition, a mouse model of diabetic nephropathy was established using a high‐fat diet and streptozotocin injection. Finally, the shRNA targeting immunoglobulin heavy constant gamma 1 (IGHG1) was introduced in vitro and in vivo to illustrate its effect on downstream factors and on the development diabetic nephropathy. Results Bioinformatics analysis revealed that IGHG1, TRIM11 (tripartite motif protein 11), and TonEBP are highly expressed in diabetic nephropathy. In vitro cell experiments demonstrated that IGHG1 positively regulates the expression of TRIM11 and TonEBP (tonicity‐responsive enhancer binding protein) in HK2 cells treated with high glucose. Furthermore, TRIM11 upregulates the expression of TonEBP through activation of the MEK/ERK (mitogen‐activated protein kinase/extracellular signal‐regulated kinase) signaling pathway in HK2 cells treated with high glucose. In vivo, animal experiments further confirmed that silencing IGHG1 could prevent the occurrence and development of diabetic nephropathy. Conclusion The silencing of IGHG1 alleviated diabetic nephropathy by inhibiting the TRIM11/MEK/ERK axis and by downregulating TonEBP.

OBJECTIVE:Alzheimer's disease (AD) is considered a neurodegenerative disease that affects the cognitive function of elderly individuals. In this study, we aimed to analyze the neuroprotective potential of isoquercetin against the in vitro and in vivo models of AD and investigated the possible underlying mechanisms. MATERIALS AND METHODS:The experimental study was performed on PC12 cells treated with lipopolysaccharide (LPS). Reactive oxygen species (ROS), antioxidant parameters, and pro-inflammatory cytokines were measured. In an in vivo approach, Wistar rats were used and divided into different groups. We carried out the Morris water test to determine the cognitive function. Biochemical parameters, antioxidant parameters, and pro-inflammatory parameters were examined. RESULTS:The non-toxic effect on PC12 cells was shown by isoquercetin. Isoquercetin significantly reduced the production of nitrate and ROS, along with the altered levels of antioxidants. Isoquercetin significantly (P<0.001) down-regulated proinflammatory cytokines in PC12 cells treated with LPS. In the in vivo approach, isoquercetintreated groups considerably showed the up-regulation in the latency and transfer latency time, as compared with AD groups. Isoquercetin significantly reduced Aβ-peptide, protein carbonyl, while enhanced the production of brainderived neurotrophic factor (BDNF) and acetylcholinesterase (AChE). Isoquercetin significantly (P<0.001) reduced pro-inflammatory cytokines and inflammatory mediators, as compared with AD groups. CONCLUSION:Based on the results, we may infer that, through antioxidant and anti-inflammatory systems, isoquercetin prevented neurochemical and neurobehavioral modifications against the model of colchicine-induced AD rats.

BACKGROUNDS:Asthma is characterized as inflammatory disorder in the respiratory system with increasing tendency. Most of the asthma patients suffered from the disease since childhood. Thus, developing novel therapeutic targets of childhood asthma is necessary. Here, we conducted the present study to investigate the effects of CTRP9 (C1q tumor necrosis factor-related protein 9), a newly identified anti-inflammatory factor, on asthma.METHODS:Sixty asthmatic children (30 moderate and 30 mild) were recruited. The mRNA level of CTRP9 in peripheral blood mononuclear cells (PBMCs) and protein level of CTRP9 in serum and induced sputum (IS) samples from asthma patients and healthy controls (HCs) were measured by qPCR and ELISA, respectively. The anti-inflammatory effects of CTRP9 was determined in vitro and potential therapeutic effect on asthma was evaluated in mouse model.RESULTS:The mRNA and protein levels of CTRP9 was significantly down-regulated in asthmatics than HCs. Furthermore, the expression level of CTRP9 was negatively correlated with the expression of TNF-α, IL-1β, and IL-6 in PBMCs. The CTRP9 significantly suppressed the expression of pro-inflammatory factors in PBMCs and sputum cells from asthma patients in vitro. And delivering CTRP9 into mouse model of asthma showed disease alleviation.CONCLUSION:Our data here indicated that CTRP9 may alleviate airway inflammation and remodeling in asthma.

目的 探究珠子参汤剂对脑胶质瘤U87细胞增殖和凋亡的影响,并对其分子机制进行初步探究.方法 将脑胶质瘤U87细胞随机分为空白组(A组)、珠子参汤荆低剂量组(B组)、珠子参汤剂中剂量组(C组)、珠子参汤剂高剂量组(D组).用MTT检测细胞增殖情况,流式细胞仪和TUNEL染色检测细胞凋亡情况,Real-time PCR检测细胞内Bcl-2 mRNA、Bax mRNA和Caspase-3 mRNA水平,Western blotting检测细胞内p-PI3K蛋白、p-AKT蛋白的水平.结果 与A组比较,C、D组细胞存活率显著降低(P＜0.05);B、C、D组Bcl-2 mRNA表达水平显著降低,B、C组Bax mRNA与Caspase-3 mRNA水平显著升高(P＜0.05);B、C、D组p-PI3K蛋白与p-AKT蛋白表达水平显著降低(P＜0.05).与B组比较,C、D组细胞存活率显著降低(P＜0.05);D组Bcl-2 mRNA表达水平显著降低,Bax mRNA与Caspase-3 mRNA水平显著升高(P＜0.05);p-PI3K蛋白与p-AKT蛋白表达水平显著降低(P＜0.05);与C组比较,D组细胞凋亡率、Bax mRNA水平显著升高,而Bcl-2 mRNA表达水平、p-AKT蛋白表达水平显著降低(P＜0.05).结论 珠子参汤剂可以抑制脑胶质瘤U87细胞增殖、细胞凋亡,其机制可能与珠子参汤剂调控PI3K/AKT信号通路有关.

目的 分析急性脑出血患者血清细胞间黏附分子1(ICAM-1)、细胞纤维连接蛋白(cFN)水平与炎性因子的相关性及预后危险因素.方法 选取2017年10月—2018年10月吉林大学第二医院神经外科诊治急性脑出血患者126例作为脑出血组,其中存活104例(存活亚组),死亡22例(死亡亚组),另选取同期在医院体检的健康志愿者50例作为健康对照组.比较2组血清ICAM-1、cFN水平及与炎性因子的相关性,分析患者死亡的危险因素.结果 脑出血组患者各个时间点的血清ICAM-1、cFN、肿瘤坏死因子-ɑ(TNF-ɑ)、白介素-1β(IL-1β)、C反应蛋白(CRP)水平均高于健康对照组(F/P=4319.339/0.000、3692.312/0.000、3862.029/0.000、621.021/0.000、899.166/0.000);患者发病3 d时的血清ICAM-1、cFN、TNF-ɑ、IL-1β、CRP水平最高,高于发病1、5 d(F/P=90.498/0.000、589.890/0.000、185.613/0.000、10.920/0.001、11.634/0.001);Pearson分析结果显示,血清ICAM-1、cFN与TNF-ɑ、IL-1β、CRP均呈正相关(ICAM-1:r/P=0.532/0.007、0.489/0.012、0.581/0.000;cFN:r/P=0.453/0.024、0.422/0.041、0.501/0.010);死亡亚组和存活亚组临床资料比较显示,血肿量、GCS评分、ICAM-1、cFN、TNF-ɑ、IL-1β、CRP差异均有统计学意义(P均<0.05),多因素Logsitic回归分析结果显示,血肿量以及血清ICAM-1、cFN、CRP水平是急性脑出血患者死亡的独立危险因素(P<0.05).结论 急性脑出血患者血清ICAM-1、cFN水平与炎性因子呈正相关,血肿量以及血清ICAM-1、cFN、CRP水平是急性脑出血患者死亡的独立危险因素.

目的 探讨D型人格对帕金森病(Parkinson's disease,PD)患者生活质量的影响.方法 便利抽样收集2015年11月至2018年2月期间在吉林大学第二医院诊治的175例PD患者作为研究对象,借助D型人格量表-14进行D型人格鉴定,并将其分为D型人格组和非D型人格组.应用非运动症状量表进行非运动症状评估,应用帕金森病调查问卷-39评估患者生活质量,应用多元线性逐步回归分析生活质量与D型人格的关系.结果 在175例参与者中,D型人格组62例(35.4％),该组低收入家庭、运动波动的患者比例较高,且生活质量总分及各领域评分均高于非D型人格组(均P<0.05);多元线性逐步回归分析显示D型人格与PD患者生活质量总分呈正相关(P<0.05).结论 D型人格的PD患者的生活质量水平显著下降.因此,掌握PD患者的D型人格特征对于制定护理策略、提高患者生活质量具有一定的指导意义.

Objective To study the classification of the abnormal muscle response (AMR) waveform in hemifacial spasm, and analyze the morphological characters and variety of AMR. Methods Clinical data of 56 patients with hemifacial spasm undergoing microvacular decompression were analyzed retrospectively. AMR examination was performed preoperatively. Muscle contraction named AMR was induced by stimulating the facial nerve branches, then, evoked potential waveforms were recorded. Different waveform morphologies were analyzed and the compression situation of the facial nerve was judged by comparing with uninjured side. Results AMR waveforms were showed in hemifacial spasm patients with microvascular compression. The classification of AMR waveform was as follows:typical waveform in 34 patients, time-limit delay type waveform in 6, scattering type waveform in 8, discontinuity scattering type waveform in 4, incremental incubation period following the stimulation intensity type waveform in 2 and diversity transmission type waveform in 2. Conclusions Preoperative AMR including many kinds of waveforms is helpful for the diagnosis of hemifacial spasm after microvascular compression, and can be used as one of indexes for judging surgery.

<正>我科曾收治1例右侧面肌痉挛、三叉神经痛及高血压三者共同发生的女性患者,行显微血管减压术(MVD)后取得良好的临床效果,该病例较少见,故进行临床分析。

我们近年收治非血管源性面肌痉挛3例,分析如下. 1 病历摘要 例1:女,18岁.以右侧面部肌肉间断抽搐10 a为主诉入院.患者于入院前10 a出现右面部肌肉抽搐,由右下眼睑开始并逐渐扩展至整个右面部.3 a来,右面部抽搐逐渐加重,查体:右侧颜面部频繁抽搐,先天性胸廓畸形.神经放射学检查:MRI显示枕骨畸形.入院诊断为右侧面肌痉挛,入院后局麻下行右侧面神经根探查术.术中见枕骨发育畸形,压迫面听神经根向脑干腹侧面移位,面听神经移至枕骨上缘,垫入Teflon棉.术后患者右侧面肌痉挛消失,出院前面肌抽搐消失,未出现并发症.随访6 a后,患者面肌抽搐消失.